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Loss of perivascular aquaporin-4 in idiopathic normal pressure hydrocephalus

Journal article
Authors M. M. Hasan-Olive
R. Enger
Hans-Arne Hansson
E. A. Nagelhus
P. K. Eide
Published in Glia
Volume 67
Issue 1
Pages 91-100
ISSN 0894-1491
Publication year 2019
Published at Institute of Biomedicine
Pages 91-100
Language en
Links dx.doi.org/10.1002/glia.23528
Keywords aquaporin-4, astrocytes, cerebrospinal fluid, glia, glymphatic, idiopathic normal pressure, retinal muller cells, immunogold cytochemistry, water transport, shunt, surgery, aqp4, polarization, deletion, localization, association, astrocytes
Subject categories Clinical Medicine

Abstract

Idiopathic normal pressure hydrocephalus (iNPH) is a subtype of dementia that may be successfully treated with cerebrospinal fluid (CSF) diversion. Recently, magnetic resonance imaging (MRI) using a MRI contrast agent as a CSF tracer revealed impaired clearance of the CSF tracer from various brain regions such as the entorhinal cortex of iNPH patients. Hampered clearance of waste solutes, for example, soluble amyloid-beta, may underlie neurodegeneration and dementia in iNPH. The goal of the present study was to explore whether iNPH is associated with altered subcellular distribution of aquaporin-4 (AQP4) water channels, which is reported to facilitate CSF circulation and paravascular glymphatic drainage of metabolites from the brain parenchyma. Cortical brain biopsies of 30 iNPH patients and 12 reference individuals were subjected to AQP4 immunogold cytochemistry. Electron microscopy revealed significantly reduced density of AQP4 water channels in astrocytic endfoot membranes along cortical microvessels in patients with iNPH versus reference subjects. There was a significant positive correlation between density of AQP4 toward endothelial cells (perivascular) and toward parenchyma, but the reduced density of AQP4 toward parenchyma was not significant in iNPH. We conclude that perivascular AQP4 expression is attenuated in iNPH, potentially contributing to impaired glymphatic circulation, and waste clearance, and subsequent neurodegeneration. Hence, restoring normal perivascular AQP4 distribution may emerge as a novel treatment strategy for iNPH.

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